An association has been established between environmental and occupational exposure to asbestos and the occurrence of neoplasms of the respiratory tract. The incidence of bronchogenic carcinoma in asbestos workers who smoke is increased significantly as compared to non-smokers. At present, the biologic mechanisms by which asbestos acts as a cocarcinogen are unclear. Experiments in this laboratory suggest that asbestos serves as a "carrier" of polycyclic hydrocarbons (PCH) into the cell. In addition, asbestos induces hyperplasia and squamous metaplasia of the respiratory tract basal cells, an effect intrinsic to carcinogenesis. This study is designed to answer the following questions: 1) Does the binding (or absorption) of PCH by asbestos relate to the structure, chemical composition and surface charge of the fiber, and does this affinity correlate with the carcinogenic potential of the asbestos? 2) What is the mechanism whereby asbestos increases the uptake of PCH by the cell and what are the structural and biochemical events in the cell that result in carcinogenic transformation? 3) Does asbestos act as a classical "tumor promoter" (i.e., does it induce nucleic acid and protein synthesis and the activity of certain characteristic enzyme systems)? Studies will be designed to assess comparatively the effects of sized preparations of crocidolite and chrysotile asbestos in assays using tracheal organ cultures, grafts of trachea in syngeneic animals and monolayers of tracheal epithelial cells.